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HEPATIC LIPIDOSIS (HL) IN CATS :cat:, FFA reached liver, 2 pathways , ,…

- - - - In most cats, the bile duct joins the single major pancreatic duct before entering the small intestine at the major duodenal papilla
      - inflammatory bowel disease (IBD)
    - - :zap: negative energy balance
        
        glucose is produced from amino acids (gluconeogenesis) and lipids are consumed for energy (β-oxidation of lipids).
  - - - lead to defective lipoprotein metabolism
        
        hepatic lipidosis
    - - HL occurs within 2 weeks
- - - - :arrow_double_down: alanine, arginine, citrulline, taurine, methionine
        
        Methionine deficiency
        
        :arrow_double_down: Methionine and its coenzyme S-adenosylmethionine for the precursors of carnitine
        
        :arrow_double_down: Enzyme carnitine palmitoyl transferase-1 that regulates
        a. ENTER of long-chain FAs into the mitochondria for β-oxidation
        b.TRANSPORT OUT FAs from hepatic cytosol into plasma
        
        :arrow_double_down: β-oxidation produces coenzyme A, which use to provide energy for Krebs cycle to produce energy or form ketone bodies
        
        Carnitine deficiency
        
        :arrow_double_down: β-oxidation ⇢ Lipid accumulation
        
        :arrow_double_down: Important thiol donor for synthesis of glutathione for hepatocellular protection
        
        :arrow_double_down: Antioxidant, :arrow_up: ROS
        
        Arginine deficiency
        
        Hyperammonemia due to decrease arginine substrate for urea cycle
        
        Hepatic encephalopathy
        
        Taurine deficiency
        
        :arrow_up: Lipolysis in peripheral tissue
        
        Low conjugation of bile acids to form bile salt (higher solubility)
  - - - :arrow_up: Counter-regulatory hormones (glucagon, growth hormone, cortisol, catecholamine)
        
        :arrow_double_down: Lipogenesis, :arrow_up: Activity of lipase ⇢ lipolysis ⇢ Mobilization of NEAFs from visceral adipose tissue to hepatocyte and store as TG
        
        :arrow_up: peripheral insulin resistance
  - - - Lack of apolipoprotein B100 (major component of VLDL)
      - Taurine, Arginine, Methionine and carnitine deficiency
- - - - Marked hyperbilirubinemia (>5 mg/dl)
      - :arrow_up: :arrow_up: Marked increases in ALT
        
        Due to altered hepatocellular membrane permeability
      - :arrow_up: :arrow_up: Marked increases in ALP (no significant rise in GGT like cholestatic disease)
        
        Cats icteric before ALP activity increases:!:
        
        :arrow_up: ALP : GGT ratio
        
        Intrahepatic cholestasis due to compression of bile canaliculi by swollen hepatocytes
    - - Due to anorexia
    - - Exacerbate the anaemia with Heinz body formation. Low phosphate ⇢ deplete ATP ⇢ increased red cell rigidity ⇢ haemolysis #
      - After insulin therapy for diabetes mellitus and following tube-feeding of anorexic cats with hepatic lipidosis (‘refeeding syndrome’)
    - - Triglyceride accumulation
        ⇢ Hepatocellular swelling
        ⇢ Compression of bile canaliculi
        ⇢ Intrahepatic cholestasis
    - - :arrow_double_down: Functional mass & :arrow_double_down: Arginine availability
    - - Due to present with inflammatory bowel diseases and pancreatitis (secondary:two:)
    - - Due to increase insulin resistance & counter-regulatory hormones (glucagon)
    - - -ve energy balance :zap:
  - - - the more critical the cat, the more care should be taken to not stress the cat with diagnostics